A Neuroecological Approach to Examining the Effects of Early Life Adversity on Adolescent Drug Use Vulnerabilities Using the ABCD Dataset

项目摘要 早期生活逆境（ELA）是神经认知风险的多维和潜在的风险因素，下游 吸毒的脆弱性以及青少年吸毒和滥用毒品。ELA对青少年吸毒风险的影响 依赖于多种动态的家庭、同龄人、学校、社区和社会文化风险和保护环境。 然而，缺乏一个重要的知识基础，以进一步了解神经系统的背景， 生物标志物影响青少年的药物风险脆弱性和行为。 新兴的研究和理论涉及支持情绪和行为的神经调节系统 监管是青少年吸毒风险调查的重点。我们关注个体差异， 神经调节系统，其中认知控制网络随着时间的推移在调节 情绪处理网络，包括情绪/显著性和奖励显著性网络。根据该 双系统观点，社会情绪网络（或ERSN，由 情感、奖励和显著性网络）和CCN会导致自我调节能力下降， 是青少年毒品风险行为的基础这种发展机制和随后的风险行为 可能会受到年轻人的尺寸压力的不同影响。现存的发育研究已经记录了 缓解ELA影响和药物使用发展的心理社会风险和保护过程 青春期的脆弱性然而，生态学方法在神经科学方法中仍然很少见。使用 发展生态神经科学的方法，我们建议调查神经认知机制， 中介，以及调节ELA对药物相关脆弱性和药物依赖性的影响的背景因素。 使用.我们将重点关注ELA对功能激活和交流的发育变化的影响 (i.e., ERSN和CCN网络之间的功能连接性（FC）及其在导致 青少年吸毒的脆弱性和后来的吸毒。 我们建议使用一个大型的纵向数据集：青少年大脑认知发展研究 (ABCD; N= 11，883;基线时年龄为9-10岁，第6波时年龄为11.5-12.5岁）。我们的目标是测试（a）发展 介导ELA对药物使用脆弱性和伴随药物使用的影响的认知机制， 滥用（B）家庭、同伴、学校、社区和社会文化背景对儿童成长的调节作用。 导致吸毒脆弱性的神经认知过程。模拟多层次的潜在变化， 行为和神经影像学数据对于进一步提高发育模型的精确性和特异性至关重要 和预防性干预项目，以提高青少年对药物成瘾的适应能力。

Project Summary Early life adversity (ELA) is a multidimensional and potent risk factor for neurocognitive risk, downstream drug use vulnerabilities, and adolescent drug use and misuse. The effects of ELA on youth’s drug use risk depend on multiple dynamic family, peer, school, community, and sociocultural risk and protective contexts. Yet, a significant knowledge base is missing to further our understanding of the contexts in which neural biomarkers affect drug risk vulnerabilities and behaviors in adolescence. Emerging research and theory implicate neuroregulatory systems that underpin emotion and behavioral regulation as a powerful focus for adolescent drug use risk investigations. We focus on individual differences in neuroregulatory systems whereby cognitive control networks become more effective over time in modulating emotion processing networks, including the emotion/salience and reward salience networks. According to this dual system view, a neuroregulatory imbalance between the socioemotional network (or ERSN, comprised of the emotional, reward, and salience networks) and CCN ushers in diminished self-regulation abilities that underlie drug risk behaviors in adolescence. This developmental mechanism and subsequent risk behaviors may be differentially affected by youth’s dimensional stress. Extant developmental studies have cataloged psychosocial risk and protective processes that moderate the impact of ELA and the development of drug use vulnerabilities in adolescence. Yet ecological approaches remain rare in neuroscience approaches. Using a developmental ecological neuroscience approach, we propose to investigate neurocognitive mechanisms that mediate, and the contextual factors that moderate, the effect of ELA on drug-related vulnerabilities and drug use. We will focus on the impact of ELA on developmental changes in functional activation and communication (i.e., functional connectivity; FC) between the ERSN and CCN networks and its mechanistic role in leading to adolescent drug use vulnerabilities and later drug use. We propose to use a large, longitudinal dataset: the Adolescent Brain Cognitive Development Study (ABCD; N=11,883; ages 9-10 at baseline and 11.5-12.5 at wave 6). We aim to test (a) the developmental cognitive mechanisms that mediate the effect of ELA on drug use vulnerabilities and attendant drug use and misuse (b) the moderating influence of family, peer, school, community, and sociocultural contexts on the neurocognitive processes that lead to drug use vulnerabilities. Modeling multilevel latent change in ecological, behavioral, and neuroimaging data is critical to further the precision and specificity of developmental models and preventative intervention programs for drug addiction resilience in adolescence.